Cerebral Venous Oxygen Saturation Research Articles

Controlled Hypoxemic Resuscitation Does Not Improve Early Cerebral Metabolic or Electrophysiological Recovery in Piglets

Background: We tested the hypothesis that controlled hypoxemic resuscitation of hypoxic newborn piglets improves early cerebral metabolic and electrophysiological recovery. Subjects: Twenty-four 2-5 days old piglets. Interventions: Hypoxia was induced by ventilating the piglets with 6% O2 in N2. When EEG became isoelectric, and either mean arterial blood pressure fell below 25 mm Hg or base excess (BE) was lower than -25 mmol/L, a 2 h resuscitation period was started. The piglets were randomly divided into three resuscitation groups: Hypoxemic (n=8), 21% O2 (n=8), and 100% O2 group (n=8). The hypoxemic group was ventilated with 12-18% O2 to achieve a cerebral venous oxygen saturation of 17-23% (baseline; 44±6%). Results: BE reached-22±6 mmol/L (mean±SE) at the end of hypoxia. PaO2 at 30 min of resuscitation were 6.0±0.4, 9.9±0.5, and 57.5±2.7 kPa in the hypoxemic, 21% O2, and 100% O2 group. No significant differences in time to recovery of EEG (p=0.17), quality of EEG at recovery (p=0.22), or extracellular hypoxanthine concentrations in cerebral cortex and striatum were found between the groups. Brain cell membrane Na+,K+-ATPase activity at the end of resuscitation was not different between the groups (p=0.30). BE and plasma hypoxanthine, however, normalized during hypoxemic resuscitation significantly slower than during resuscitation with 21% or 100% O2.Conclusion: Controlled hypoxemic resuscitation did not improve early brain recovery compared with resuscitation with 21% and 100% O2, and showed a delayed metabolic correction of the total body hypoxia. In contrast, resuscitation with 21% O2 was as efficient as resuscitation with 100% O2 in this newborn piglet hypoxia model.

The Brain Uses Mostly Dissolved Oxygen During Profoundly Hypothermic Cardiopulmonary Bypass

Background. During profoundly hypothermic cardiopulmonary bypass, cerebral venous oxygen saturation increases (eg, to 98% at 15°C). We reanalyzed results of clinical studies to learn why.Methods. One hundred sixty-eight cerebral oxygen transport measurements were available from 96 infants and children undergoing profoundly hypothermic cardiopulmonary bypass during repair of congenital heart defects.Results. Dissolved oxygen accounted for 2% to 17% of arterial oxygen content, depending on the arterial oxygen partial pressure and hemoglobin concentration. The fraction of the cerebral metabolic rate for oxygen obtained from dissolved oxygen depended on pump flow, temperature, hemoglobin concentration, and arterial oxygen partial pressure (all p < 10−3). For “full-flow” cardiopulmonary bypass, temperatures less than 18°C, and arterial oxygen partial pressure measurements more than 180 mm Hg, the mean ± standard deviation of the fraction of cerebral metabolic rate for oxygen obtained from dissolved oxygen equaled 77% ± 19%.Conclusions. Dissolved oxygen satisfies most of the brain’s oxygen requirements during profound hypothermic cardiopulmonary bypass. This result reflects four properties of profound hypothermic cardiopulmonary bypass: (1) increases in hemoglobin’s oxygen affinity due to profound hypothermia (which impairs oxygen transfer from hemoglobin to cerebral tissue), (2) use of hemodilution, (3) use of high arterial oxygen partial pressure, and (4) low cerebral metabolic rate of oxygen.(Ann Thorac Surg 1997;63:1725–9)

Neurophysiologic monitoring to assure delivery of retrograde cerebral perfusion

Background: Patients undergoing complex aortic procedures performed with deep hypothermia and circulatory arrest have a significant risk of an adverse neurologic event when the arrest period is prolonged. Retrograde cerebral perfusion appears to improve cerebral protection, although collapsed cortical veins or functional jugular venous valves may restrict flow at the frequently recommended maximum pressure of 25 mm Hg. Therefore, the purpose of this study was to demonstrate the benefit of multimodality neurophysiologic monitoring in assuring delivery of retrograde cerebral perfusion. Methods: Electroencephalography, cerebral blood flow velocity, and regional cerebral venous oxygen saturation were used to quantify the intraoperative neurophysiologic changes accompanying retrograde cerebral perfusion. The magnitude of changes was compared with those previously observed during arrest without retrograde cerebral perfusion. Results: Thirty patients underwent complex aortic procedures necessitating circulatory arrest, 22 with retrograde cerebral perfusion. The mean retrograde perfusion pressure of 40 mm Hg (30 to 49 mm Hg, 95% confidence interval) and flow rate of 1.2 L/min (0.9 to 1.6 L/min) necessary to achieve documented retrograde cerebral perfusion was much higher than previously recommended. During both retrograde cerebral perfusion and rewarming, cerebral oximetric monitoring guided adjustments in perfusion parameters to limit the rate of desaturation to 0.4% per minute (0.3% to 0.6%). With retrograde cerebral perfusion there was a rapid (1) recovery of electroencephalographic activity during rewarming (21 minutes [range 16 to 26 minutes]) and (2) return of consciousness after the operation (81% [58% to 95%, 95% confidence interval] awake by 12 hours). There was no transcranial Doppler evidence of cerebral edema with retrograde cerebral perfusion. Two neurologic complications occurred in the 22 patients managed with retrograde cerebral perfusion and one in the eight patients managed with arrest only. Conclusions: Multimodality neurologic monitoring assured optimal brain cooling and bihemispheric delivery of retrograde cerebral perfusion. Necessary retrograde pressure and flow were often higher than values previously reported. Avoidance of profound cerebral venous oxygen desaturation during retrograde cerebral perfusion and rewarming was associated with rapid recovery of neurologic function. (J Thorac Cardiovasc Surg 1997;113:748-57)

Significance of elevated cytochrome aa3 in a state of endotoxemia in dogs

It is now possible to detect quantitative changes in cytochrome aa 3 by means of near-infrared spectrophotometry. This technique is also suitable for determining oxidised hemoglobin (HbO 2), reduced hemoglobin (Hb), cerebral blood volume, and the redox state of cytochrome aa 3 (cyt aa 3) in the tissues. The significance of elevated cyt aa 3, measured by near-infrared spectrophotometry, is still unclear, so we investigated this question using both near-infrared spectrophotometry and oxygen saturation meters in endotoxemic dogs. Ten anaesthetised mongrel dogs were injected with endotoxin ( E. coli 0111: B4 Difco 2 mg/kg i.v.) and the redox state of Hb and cyt aa 3 was determined in real time by near-infrared spectrophotometry. The levels of arterial and cisternal venous oxygen saturation were recorded simultaneously by two Oximetrix 3 saturation meters to calculate the cerebral arterial and venous oxygen saturation difference (Sata-vO 2D) in real time. HbO 2 decreased along with the fall in mean arterial pressure and remained at a low level, while Hb increased aad remained at a high level. The cerebral blood volume decreased in the endotoxic early stage and then returned gradually towards baseline. Cyt aa 3 showed an increase following endotoxin injection and maintained an oxidised form. The cerebral Sata-vO 2D rose to about three times the control level. From these observations, an increase of oxidised cytochrome aa 3 after endotoxin administration seems to be a compensatory protective effect in response to the cerebral oxygen demand rather than over-oxygenation or hyperoxia.

Theoretical Analysis of Cerebral Venous Blood Hemoglobin Oxygen Saturation as an Index of Cerebral Oxygenation During Hypothermic Cardiopulmonary Bypass

BackgroundJugular venous catheters and near-infrared spectroscopy can measure cerebral venous blood hemoglobin oxygen saturation (SvO 2). We used computer simulation to characterize the relation between Sv sub O2 and cerebral metabolic rate for oxygen (CMRO2) during hypothermic cardiopulmonary bypas

Cerebral hyperthermia during cardiopulmonary bypass in adults

Accepted for publication June 7, 1995 In this report, we document that cerebral hyperthermia occurs regularly during rewarming from hypothermic cardiopulmonary bypass (CPB). These high brain temperatures are not adequately reflected by nasopharyngeal (NP) temperature and may contribute to neurologic morbidity. Stroke and neurocognitive injury remain significant components of perioperative morbidity associated with cardiac surgery. Hypothermic CPB is used in part for its cerebral protective effects. Recent reports, however, have indicated that the rewarming phase of hypothermic CPB is associated with a significant incidence of decreased cerebral venous oxygen saturation (Sjvo2; 50%). 1,2 Sjvo2 is thought to be a general index of the adequacy of the matching of cerebral oxygen supply with demand.

The role of neuromonitoring in cardiovascular surgery

This review describes the techniques currently used for quantitative neurophysiologic measurement during cardiac surgery and their potential impact on clinical outcome. Electroencephalography (EEG) characterizes cerebrocortical neuronal electrical activity and was part of some of the earliest cardiopulmonary bypass procedures, yet today it is not in widespread use. Each of the common misunderstandings regarding a supposed limitation of this technology is explained. Its major genuine shortcoming, a lack of selectivity, may now be overcome with the combined use of additional monitoring modalities. The influence of intracranial hemodynamics on observed EEG changes may be determined continuously and noninvasively with transcranial Doppler (TCD) ultrasound. TCD provides an indication of sudden change in either blood flow or vascular resistance as well as the detection of emboli. In addition, the metabolic status of cortical neurons can be monitored by regional cerebral venous oxygen saturation (rCVOS) using noninvasive transcranial near-infrared spectroscopy. The % rCVOS tends to remain remarkably stable over a wide range of temperatures, perfusion pressures, and anesthetic states. Marked change in either direction signifies a serious imbalance between oxygen delivery and consumption. Measurement of rCVOS does not require blood flow, pulsatile or otherwise, so that it offers the only means of monitoring during circulatory arrest. By characterizing the dynamic interplay among cerebral hemodynamics, metabolism, and electrogenesis, these technologies permit the rapid detection and correction of potentially hazardous conditions.

Theoretical Analysis of Cerebral Venous Blood Hemoglobin Oxygen Saturation as an Index of Cerebral Oxygenation during Hypothermic Cardiopulmonary Bypass

Jugular venous catheters and near-infrared spectroscopy can measure cerebral venous blood hemoglobin oxygen saturation (SvO2). We used computer simulation to characterize the relation between Sv02 and cerebral metabolic rate for oxygen (CMR02) during hypothermic cardiopulmonary bypass (CPB). We developed a theoretical model of cerebral oxygen consumption and blood-brain oxygen transfer. Our model included the temperature dependence of blood and brain oxygen solubility; the temperature, age, and acid-base dependence of hemoglobin oxygen dissociation; and the temperature and age dependence of CMRO2. We simulated cerebral blood flow reductions that decreased Sv02 and CMR02. Our model predicts the relation between CMR02 and Sv02 to be dependent on temperature, because of a shift of the oxygen partial pressure at which hemoglobin oxygen saturation equals 0.50. For example, during normothermic CPB, Sv02 can decrease to 30% before CMR02 will decrease to less than 90% of normal. In contrast, for alpha-stat management of infants at 17 degrees C, Sv02 must be maintained at greater than 95% to maintain CMR02 at greater than 90% of its temperature appropriate value. High Sv02 observed during hypothermic CPB may indicate impaired oxygen transfer from hemoglobin to brain, not "luxury perfusion." The relation between Sv02 and CMR02 depends dramatically on the temperature of the patient. Sv02 per se may not be reliable index of normal CMR02 during hypothermic CPB.

Light-reflective cerebral oximetry and jugular bulb venous oxygen saturation during carotid endarterectomy

Light-reflective cerebral oximetry and jugular bulb venous oxygen saturation during carotid endarterectomy

A prospective, randomized comparison of cerebral venous oxygen saturation during normothermic and hypothermic cardiopulmonary bypass : Cook DJ, Oliver WC Jr, Orszulak TA, Daly RC J Thorac Cardiovasc Surg 107: 1020–1029, 1994

A prospective, randomized comparison of cerebral venous oxygen saturation during normothermic and hypothermic cardiopulmonary bypass : Cook DJ, Oliver WC Jr, Orszulak TA, Daly RC J Thorac Cardiovasc Surg 107: 1020–1029, 1994

Evaluation of a 7.5 French Pulmonary Catheter for Continuous Monitoring of Cerebral Venous Oxygen Saturation

We studied a 7.5 French Opticat fiberoptic catheter/Oximetrix computer system as a tool for continuous monitoring of oxygen saturation of jugular venous blood. Eight healthy volunteers had a catheter placed with the tip in the bulb of the right internal jugular vein. During baseline condition, hyperventilation, and rebreathing, jugular venous oxygen saturations ranging from 35 to 85% were obtained. Simultaneous with drawing a blood sample, the value obtained with the fiberoptic catheter was recorded. The oxygen saturation of the blood sample was analyzed in vitro using a bench oximeter. A total of 150 paired values was obtained. In 15 of these cases, the computer indicated that the intensity of the reflected light was insufficient. A difference of > 12% oxygen saturation between the paired values was obtained for all of these pairs. The regression coefficient for the remaining 135 data pairs was 0.95, the mean difference was -0.54%, and the limits of agreement were -9.5 to 8.4%. We conclude that the 7.5 French Opticat catheter is useful if values obtained during improper light intensity are excluded.

255 MEASUREMENT OF CEREBRAL VENOUS SATURATION BY NEAR INFRARED ABSORPTION SPECTROSCOPY

Method :- Near Infra-Red Absorption Spectroscopy (NIRAS, Hamamatsu NIRO 500) was performed on the heads of four children undergoing cardiac catheterisation. An increase in cerebral blood volume was achieved by unilateral jugular venous occlusion for about 5 seconds. Cerebral venous oxygen saturation (CSvO2) by NIRAS was calculated and compared with direct measurement by co-oximetry of blood from the internal jugular vein.

A prospective, randomized comparison of cerebral venous oxygen saturation during normothermic and hypothermic cardiopulmonary bypass

Recent reports have described cerebral venous oxygen desaturation during and after rewarming from hypothermic cardiopulmonary bypass. Additionally, patients undergoing normothermic cardiopulmonary bypass may be at higher risk for neurologic injury. This study was designed to determine whether patients undergoing normothermic cardiopulmonary bypass are at increased risk for sustained cerebral desaturation. Fifty-two patients undergoing first-time coronary artery bypass grafting were randomized to receive normothermic (37 degrees C, n = 26) or hypothermic (27 degrees C, n = 26) cardiopulmonary bypass. The anesthetic was standardized and alpha-stat pH management was used. A 4F oximetric catheter was placed in the jugular bulb and cerebral venous and radial arterial blood were sampled. Oxygen partial pressure and saturation were measured at six intervals from cerebral venous blood and from radial arterial blood. Patients receiving normothermic cardiopulmonary bypass had lesser values of oxygen partial pressure and saturation in cerebral venous blood than patients subjected to hypothermia during the first 40 minutes of bypass. Cerebral venous desaturation (oxygen saturation in cerebral venous blood of 50% or less) was observed in 54% of patients in the normothermic group and 12% of patients in the hypothermic group during cardiopulmonary bypass. In the normothermic group, cerebral desaturation occurred primarily in early bypass (14 of 26). The three episodes of desaturation in the hypothermic group occurred during rewarming. During cardiopulmonary bypass, the arteriovenous oxygen content difference was greater in the normothermic group than in that in the hypothermic group, suggesting higher oxygen consumption. Differences in glucose utilization during early cardiopulmonary bypass between the groups was also detected. One patient in the hypothermic group had an embolic stroke and subsequently died. There were no other perioperative strokes or deaths in the study population. The present study demonstrates that patients undergoing normothermic cardiopulmonary bypass are at greater risk for cerebral desaturation. Because it is a global assessment, cerebral venous oxygen saturation may be insensitive to focal ischemic events. It remains to be seen whether these differences in cerebral physiologic states translate into differences in clinical outcome.

Cerebral Venous Oxygen Saturation Studied with Bilateral Samples in the Internal Jugular Veins

The current literature reports many measurements (arteriovenous oxygen content difference and cerebral metabolic rate of oxygen, etc.) with samples from the internal jugular veins (IJs), obtained from either side of the neck, based on the assumption that a reliable sample of mixed venous blood can be drawn. We compared oxygen saturation in both IJs in 32 patients with head injuries to establish the similarities or discrepancies in the two veins. Both IJs were cannulated with 20-G catheters; in five patients, a fiberoptic catheter was used to obtain a continuous recording of the hemoglobin saturation. Blood samples were taken simultaneously from the two IJs and immediately processed; the total number of samples processed was 342, with an average of 5.34 paired samples from each patient. The mean and the standard deviation of the differences between the saturation of the two IJs were, respectively, 5.32 and 5.15. Fifteen patients showed differences greater than 15% in hemoglobin saturation; three more patients showed differences greater than 10% at some point during the investigation. Ultimately, only eight patients had differences of less than 5%. No relationship was found among the computed tomographic scan data and the pattern of hemoglobin saturation detected. Therefore, we were not able to identify the side more appropriate for monitoring in patients with bilateral, predominantly monolateral, cortical, or deeply located lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral Venous Oxygen Saturation Studied with Bilateral Samples in the Internal Jugular Veins

Cerebral Venous Oxygen Saturation Studied with Bilateral Samples in the Internal Jugular Veins

Estimation of Cerebral Venous Saturation in Newborn Infants by Near Infrared Spectroscopy

The purpose of the study was to evaluate the near infrared spectroscopy technique for determination of the cerebral venous oxygen saturation. By tilting the patient's head down 15 degrees, changes in OD may be caused by changes in cerebral blood volume. On the assumption that increases in cerebral blood volume consist of venous blood only, cerebral venous oxygen saturation can be calculated as the measured change in oxygenated Hb divided by the change in total Hb. Two groups of mechanically ventilated, newborn infants were investigated: 10 asphyxiated, term infants and another 22 preterm infants with respiratory distress syndrome. All were monitored by near infrared spectroscopy during tilting, and cerebral blood flow was estimated by the 133Xe clearance technique immediately before tilting. Cerebral venous oxygen saturation could not be calculated in 13 preterm infants, as the blood volume remained constant during tilting. In the remaining 19, cerebral venous oxygen saturation averaged 0.67 (SD = 0.09) in asphyxiated infants and 0.53 (SD = 0.15) in preterm infants (p = 0.03). The corresponding values of cerebral blood flow were closely and inversely related to oxygen extraction calculated from cerebral venous saturation as estimated by near infrared spectroscopy.

Relationship between cerebral blood flow velocity and cerebral venous oxygen saturation during hypothermic cardiopulmonary bypass

Relationship between cerebral blood flow velocity and cerebral venous oxygen saturation during hypothermic cardiopulmonary bypass

Cerebral oxygen consumption and blood flow in Fischer-344 rats of different ages

Regional cerebral oxygen consumption and blood flow were determined and compared in conscious male Fischer-344 rats at 3, 12, 24 and 33 months of age to correlate the reported regional neurochemical and morphological changes which occur in these parameters during development, maturation, aging and senescence. Cerebral blood flow was determined with 14[C]-labelled iodoantipyrine and regional cerebral arterial and venous oxygen saturation was measured microspectrophotometrically. Oxygen consumption was obtained by multiplying cerebral blood flow and oxygen extraction. Systolic and diastolic blood pressure and heart rate decreased significantly with age. A Average cerebral blood flow, oxygen extraction and oxygen consumption/100 g did not differ significantly between the four age groups examined. Oxygen consumption averaged 2.9±0.1 ml O 2/min/100 g (mean±S.E.M.) in the 3-month-old group and 3.6±0.1 ml O 2/min/100 g in the 33-month-old group. Differences in flow among the examined brain regions, which were present in the mature, 12-month-old brain, were not present in the developing, aging or senescent rat brain. Compensatory alterations in the efficiency or organization of neurochemical activity which occur during development, aging and senescence may modify the inter-regional differences in cerebral blood flow and oxygen consumption noted during maturation. There was no correlation found between the neurochemical and morphological changes which have been reported during maturation, aging or senescence and regional cerebral oxygen consumption.

Effect of withdrawal from chronic naltrexone on regional cerebral oxygen consumption in the cat

This investigation determined the effects of withdrawal from chronic naltrexone administration on average and regional cerebral blood flow, oxygen extraction and oxygen consumption. The relationship between the effects of withdrawal from chronic administration of this opiate receptor antagonist, which may increase the numbers of postsynaptic opiate receptors, and these parameters was investigated. Fourteen adult mongrel cats were administered subcutaneous injections of 1 mg/kg naltrexone HCl or 1 ml 0.9% saline twice daily for 21 days. Two days later, regional cerebral blood flow was monitored using radioactively tagged microspheres. The animals were sacrificed and prepared for microspectrophotometric analysis of regional cerebral venous and arterial oxygen saturation. Regional cerebral oxygen consumption was calculated as the product of cerebral blood flow and oxygen extraction for each area examined. After 2 days of withdrawal from chronic naltrexone treatment, the blood pressure, heart rate and blood gas parameters did not change significantly when compared to saline-treated animals. Average cerebral blood flow was significantly increased from 47.9 ± 3.4ml/min/100 g (mean ± S.E.M.) in the control group to 80.3 ± 6.5 (ml/min/100 g) in the chronic naltrexone-treated group. Flow was significantly increased in the cortex, lenticulate nuclei, thalamus and pons. Neither average cerebral oxygen consumption, which increased slightly, nor cerebral oxygen extraction, which decreased slightly, were significantly altered by treatment. The distribution of flow among the examined regions was, however, significantly altered in the animals 2 days after receiving chronic naltrexone injections. These changes were not restricted to brain regions dense in neuronal opiate receptors. There was no relationship between the increased number of opiate receptors, which have been reported to occur during and immediately after treatment with naltrexone, and cerebral oxygen consumption. Withdrawal from chronic naltrexone administration may have a direct effect on the cerebral vasculature.

Effect of morphine on regional cerebral oxygen consumption and supply

The effects of acute opiate receptor stimulation on regional cerebral oxygen consumptilon and blood flow were examined in 9 regions of the artificially respired, α-chloralose-anesthetized cat. Regional cerebral arterial and venous oxygen saturation were examined microspectrophotometrically and regional cerebral blood flow was monitored using radioactively tagged microspheres (15 ± 3 μm in diameter). Oxygen consumption was calculated as the product of flow and oxygen extraction. In 8 cats, after control cerebral blood flow was obtained, and in 8 experimental cats after this same measurement was obtained before and 40 min after the administration of 1.5 mg/kg morphine sulfate; the cats' heads were simultaneously sawed in 3 places and quickly frozen in liquid nitrogen-cooled propane. Systolic and diastolic blood pressure were significantly decreased by treatment. The heterogeneity of venous oxygen saturation was significantly reduced by morphine. Average cerebral blood flow, oxygen extraction and consumption were not altered significantly by morphine. Regional cerebral blood flow in the hypothalamus, thalamic oxygen extraction, and hypothalamic and thalamic oxygen consumption were significantly decreased by treatment. This low dose of morphine may produce changes in cerebral neuronal and/or synthetic activity which lowers oxygen consumption in some regions rich in opiate receptors, while not affecting overall brain oxygen supply or consumption.